Saccades

1. Saccades

2. Saccades • field changing movements • used voluntarily, as well as in response to visual and other sensory stimuli • redirect the visual axis to permit changes in the direction of fixation independent of head movements • routinely used in clinical tests of oculomotor function

3. Quick phases • involuntary saccades • brainstem pathways used to generate saccades are also responsible for quick phases

4. Latency • period from the onset of the eccentric target to the beginning of the saccade • about 200-250 milliseconds • somewhat longer for larger saccades. • If no fixation point, latencies are considerably shorter • 100-120 milliseconds • called “express saccades” • depend on different neural pathways

5. Sampled control • Once initiated, normal saccades cannot be altered in direction or extent • Brain seems to “decide” on one saccade, execute it, and then determine if another saccade is needed to get to any given target • saccadic system seems to “sample” the environment periodically, not continuously

6. Velocity and duration • extremely high velocities, short durations • greater than 700° per second • velocity and duration depend on amplitude • functions depicting the relationship of velocity and duration to amplitude • “main sequence diagrams” • define normal saccades

7. Main sequence diagrams • For a given amplitude, expect • little variability in either duration or velocity • Saccades not failing on the main sequence diagrams may not be normal • warrant further investigation or a referral

8. Pulse and step • Oculomotor motor neurons • pulse (rapid burst of action potentials) causes saccade • Larger pulses produce higher velocities • larger saccades are faster because motor neurons fire more rapidly • Duration of pulse determines duration of saccade • Larger saccades take longer because the motor neurons fire longer

9. Step • Step: increase in neural firing to give the EOM force necessary to hold the eye in the new position • produced by a neural integrator that integrates the pulse • maintains proper calibration between the size of the pulse and the size of the step

10. Without the step, the pulse could relocate the eye • could not maintain eccentric eye position • resulting in a nystagmus as the eye first relocated, drifted toward center, relocated again, and so forth. • Without the pulse, the step would give slow movements only (like vergences) with exponential drift to new position

11. How does the brain generate the pulse and step signals? Where do they arise?

12. Reticular Formation • PPRF (paramedian pontine reticular formation) • staging area for horizontal saccades and quick phases • mesencephalic reticular formation • machinery for generating vertical saccades and quick phases • Oblique saccades require coordination between these two areas.

13. Burst neurons • cause of pulse for ipsilaterally- directed saccades and quick phases in the motor neurons • project to both abducens motor neurons and to internuclear neurons • lesions of the VIth Nucleus cause paralysis of the ipsilateral lateral rectusand the contralateral medial rectus • VI nerve lesions affect the ipsilateral lateral rectus only

14. Pause neurons • located near the abducens nucleus • discharge continuously except just before saccades, when they pause • pause begins slightly before each saccade and continues for duration of the saccade • pause cells seem to inhibit burst cells

15. Tonic neurons • discharge as a function of eye position • thought to be the output of the “Neural Integrator” • necessary for the step of firing in motoneurons

16. D.A. Robinson’s local feedback model of saccadic system

17. Medial Longitudinal Fasiculus (MLF) • Unilateral lesions • paralysis of adduction in the ipsilateral eye for all conjugate eye movements (vestibular as well as voluntary) • sent to the MR subdivision of the III nucleus • from interneurons of the Abducens nucleus (VI)

18. MLF • Lesions of MLF spare convergence eye movements • convergence signals must come from the rostral brainstem • above the site of the MLF lesion

19. Superior colliculus • causes contralaterally-directed saccades • mapped topographically in SC in correspondence to the visual map: • upward saccades are represented medially, as is the upper visual field • downward saccades are represented laterally, as is the lower visual field • small saccades are represented anteriorly • larger saccades are represented caudally, as is the peripheral contralateral visual field.

20. Damage to superior colliculus • transient deficits in responding to targets in the contralateral visual field • longer lasting neglect of targets • increases in the latency of saccades to visual targets in the affected portion of the visual field • decreases in accuracy • hypometria or undershooting

21. Frontal Eye Fields (FEF) • location generally • lateral part of precentral sulcus • close to the area of motor cortex activated by hand movements • Brodmann areas 6 and 4. • stimulation produces conjugate, contralateral deviations of the eyes • lesions transiently disturb the ability to make voluntary contralaterally-directed saccades

22. FEF and SC • Damage to both FEF and SC • permanent saccadic paralysis • FEF and SC are parallel pathways to brainstem mechanisms for generating saccades

23. Visual Neglect • Aka unilateral neglect • Classical cases: damage in posterior parietal cortex • Other brain areas in which damage causes neglect : • superior colliculus • frontal eye fields • = areas involved in voluntary eye movements, particularly saccades

24. Symptoms of neglect • Copying only one half of familiar objects • drawing only the right side of a clock or face • Combing only the right side of his or her hair • Men: shaving the right side of the face • Women: applying makeup only on the right

25. Sidedness of neglect • right hemisphere damage usually causes more severe neglect than does left hemisphere damage • may be related to specialization of the right hemisphere for visual spatial processing

26. Is neglect a visual field defect? • Probably not • Usually no scotoma • Relates to one half of familiar objects, regardless of where the patient looks • Has some attentional features • patients may report a stimulus if his or her attention is drawn to it

27. Saccadic Suppression • We are less able to detect dim targets for a short period of time around saccadic eye movements • suppression of vision begins before the eyes actually start to move • continues after they are steady again • thresholds for detecting visual stimuli are elevated when compared to thresholds obtained during fixation

28. 3 explanations for suppression • retinal • saccades are so fast that they affect retinal function • visual masking • successively presented contours interfere with each other • effort of will (or corollary discharge) • elevates visual thresholds.

29. Facts about saccadic suppression • begins about 100 milliseconds before saccade onset and terminates about 100 milliseconds after the end of a saccade • seems to eliminate retinal responsibility for the presaccadic effects • occurs in contourless environments (a Ganzfeld) • seems to eliminate visual masking as necessary for suppression

30. With other causes unlikely, effort of will corollary discharge is the most likely explanation for saccadic suppression

31. Saccadic Adaptation • saccades can be modified in response to peripheral changes • Like VOR • two types of changes • Muscle palsy • anisometric spectacles

32. Muscle palsy • saccades can be accurate in only one of the eyes • If paretic eye is used for fixation • it will have accurate saccades even in the direction of muscle weakness • saccades in the nonparetic eye will be too large (hypermetric) and have post-saccadic drift • thought to result from a pulse-step mismatch

33. Patients with muscle palsy • saccadic innervation is apparently readjusted in both eyes because of Hering’s law • improves saccadic performance of the habitually viewing eye but degrades the performance the fellow eye.

34. Patients with muscle palsy • changes are conjugate • changes are not permanent • eye normally used for viewing will be accurate • that eye is patched, the other becomes more accurate while the originally preferred becomes less accurate

35. Nonconjugateadaptation of saccades • seen in patients exposed to anisometric spectacles • saccades become different in size in the two eyes • smaller amounts of anisometropia (2D) lead • rapid adaptation • larger amounts of anisometropia (6D) • slower adaptation

36. Adaptation to anisometropic spectacles • nonconjugate adaptation in smooth pursuit eye movements and saccades • changes occur during both monocular and binocular viewing • basic programming of eye movements has been changed by exposure to different size images in the two eyes

38. Synthesis of conjugate signals • horizontal versional movements • organized in pontine tegmentum near the abducens nucleus • abducens nucleus contains two populations of neurons • abducens motor neurons project to the ipsilateral LR • abducens internuclear neurons project up the contralateral MLF to MR motor neurons in the IIIrd nucleus

40. Lesions of the abducens nucleus • cause paralysis of the ipsilateral lateral rectus and the contralateral medial rectus for all conjugate movements • spare vergence eye movements

41. Vestibular afferents from the horizontal semicircular canals project mainly to the medial vestibular nucleus (MVN) • MVN projects to contralateral abducens (VI) nucleus. • damage to the abducens nucleus will disrupt the vestibulo-ocular and optokinetic reflexes

42. PPRF damage • generally produces ipsilateral conjugate horizontal gaze palsy • always for rapid movements; often for slow movements • for both voluntary or reflexive

43. Vertical versional movements • organized in the rostral mesencephalon • riMLF or rostral interstitial nucleus of the MLF • INC or the interstitial nucleus of Cajal • anterior to the oculomotor nucleus • bilateral damage causes deficits in vertical movement but spares horizontal movement

45. Vertical burst neurons • Vertical BNs of MRF • upward burst neurons project to motor neurons for the superior rectus and inferior oblique muscles of both eyes • downward BNs project to motor neurons for the inferior rectus and superior oblique of both eyes • structural basis for Hering’s law as it applies to vertical eye movements.

46. Vertical deficits • saccades • smooth pursuit • vestibular and OKN • maintenance of vertical eye position